Methylator resistance mediated by mismatch repair deficiency in a glioblastoma multiforme xenograft

A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1997-07, Vol.57 (14), p.2933-2936
Main Authors: FRIEDMAN, H. S, JOHNSON, S. P, GERMAIN, G, DRUMMOND, J. T, KEIR, S, MARCELLI, S, BIGNER, D. D, MODRICH, P, DONG, Q, SCHOLD, S. C, AHMED RASHEED, B. K, BIGNER, S. H, ALI-OSMAN, F, DOLAN, E, COLVIN, O. M, HOUGHTON, P
Format: Article
Language:English
Subjects:
Animals
Antineoplastic agents
Biological and medical sciences
DNA Methylation
DNA Repair
Drug Resistance
General aspects
Glioblastoma - drug therapy
Glioblastoma - genetics
Humans
Medical sciences
Melanocyte-Stimulating Hormones - analysis
Methyltransferases - metabolism
Mice
Mice, Inbred BALB C
Microsatellite Repeats
Neoplasm Transplantation
O-Methylguanine-DNA Methyltransferase
Pharmacology. Drug treatments
Transplantation, Heterologous
Tumor Cells, Cultured
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Summary:A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotecan, CPT-11, cyclophosphamide, and busulfan. D-245 MG (PR) xenografts were resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to the other agents. Both D-245 MG and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathione and glutathione-S-transferase were similar. D-245 MG xenografts expressed the human mismatch repair proteins hMSH2 and hMLH1, whereas D-245 MG (PR) expressed hMLH1 but not hMSH2.
ISSN:0008-5472
1538-7445